Retroviruses induce a variety of tumors in vertebrates. A host origin for retroviral oncogenes is implied by the discovery that vertebrate DNA contains highly conserved genes (denoted "c-oncs") that are homologous to retroviral oncogenes. Recent studies in several laboratories suggest that activation of c-oncs may play a role in the induction of numerous kinds of malignancies. The similarity between viral oncogenes and c-onc genes implies a normal role for c-onc proteins in growth control and/or differentiation. The long-term aim of my program is to elucidate the presumptive roles of c-oncs as cancer genes and as regulators of normal cell growth. My work focuses primarily on the investigation of a possible role for one of the c-oncs, c-myb, in the differentiation of T lymphocytes. In previous work with chickens, we demonstrated that hematopoietic organs, especially the thymus, are enriched for expression of c-myb. In current studies with mice, we have so far shown that (1)\hematopoietic organs (thymus, spleen, mesenteric lymph nodes, bone marrow, fetal liver) contain detectable c-myb mRNA, but that kidney, brain, adult liver, and heart do not; (2)\in mice ranging from newborns through 8 months of age, the amount of c-myb mRNA is greatest for the thymus and is 5-\to 10-fold higher in the thymus than in the spleen; for both organs, the amount of c-myb mRNA peaks at 1 to 2 weeks of age; (3)\cell fractionation studies suggest that the less mature thymic lymphocytes are somewhat enriched for c-myb mRNA. These findings, in summary, are consistent with the possibility that expression of c-myb is elevated in the earlier stages of the T-lymphocyte lineage and then declines as these cells mature. These observations suggest that c-myb may play a role in differentiation of T lymphocytes. Also, efforts are under way to clone and sequence the mouse c-myb gene. Within a few months, we will initiate similar studies on the expression of several other c-onc genes.